Patients with Bartter's syndrome are resistant to the pressor effects of angiotensin II and norepinephrine. This increase in resistance to angiotensin II and norepinephrine is associated with an overproduction of prostaglandins and is corrected by treatment with a prostaglandin synthetase inhibitor. Recently, we have shown that the increase in pressor resistance to norepinephrine of patients with Bartter's syndrome is associated with an increased excretion of norepinephrine in the urine. This increased excretion of norepinephrine may reflect an increase in activity of the sympathetic nervous system occurring in response to the increase in pressor resistance to norepinephrine. A normal to borderline high excretion of the metabolites VMA and metanephrine and restoration of urinary norepinephrine to normal by inhibition of prostaglandin synthesis supports the hypothesis of an increase in sympathetic nervous system activity mediated by prostaglandins.